Chapter 9 Kidney Disease Flashcards
Diagnosis and screening to determine kidney diseases
- Abnormality in biochemical blood screen
- functional change in glomerular filtration rate (GFR)
- abnormality in urinalysis: proteinuria and hematuria
- systemic disease with renal involvement: diabetes mellitus
- symptom, physical sign, imaging
- kidney biopsy
Major types based on where kidney was initially affected
- Glomerular
- Tubular
- Interstitial
- Vascular
What major type is most often immune related?
Glomerular
What major type affects proximal/distal tubules and is a result from toxic or infectious substances
Tubular
What major type is damage from neglected UTIs and result from toxic or infectious substances
Interstitial
What major type affects blood flow from the heart and reduces renal perfusion?
Vascular
Types of glomerular disorders and morphologic changes
Distinct changes/damage: - immunologic - non-immunologic Types: - primary immunologic - Secondary to systemic diseases - hereditary
Immune mediated changes in glomerulus
- Cellular proliferation: increased numbers of endothelial and other cells
- Leukocyte infiltration
- glomerular basement membrane thickening: immune complexes and diabetes
- Hyalinization with sclerosis (scarring)
Clinical features of nephritis vs nephrotic diseases
- Hematuria
- proteinuria
- Lipiduria
- oliguria
- Azotemia (increased blood urea nitrogen)
- Edema
- Hypertension
2 glomerular diseases
Nephritic and nephrotic: acute, chronic
Features of nephrotic syndrome
- Onset: insidious
- Edema: ++++
- Blood pressure: normal
- jugular venous pressure:normal/low
- Proteinuria: ++++
- Hematuria: may/may not occur
- red blood cell casts: absent
- serum albumin: low
Features of nephritic syndrome
- Onset: abrupt
- edema: ++
- blood pressure: raised
- jugular venous pressure: raised
- proteinuria: ++
- hematura: +++
- Red blood cell casts: present
- serum albumin: normal/ slightly reduced
Cause of nephrotic syndrome
Increased permeability of the glomerular due to damage of basal Lamina and podocytes. Massive loss of protein (mostly albumin) in urine
Clinical findings of nephrotic syndrome
Pronounced soft and pitting edema and hyperlipidemia
Urinalysis of nephrotic syndrome
Cloudy, fat droplets
- protein > 3.5g/day and 4+ positive on dipstick
- lipiduria
- oily
Microscopic findings of nephrotic syndrome
- Oval fat bodies, free fat globes
- increased renal tubular epithelial cells
- increased casts: all types, particularly fatty, waxy, and renal well
Cause of acute post streptococcal glomerutonephritis
Sudden onset occurs 1-2 weeks after group A beta-hemolytic strep with M protein infection of throat or skin (strep throat)
Clinical findings of acute post streptococcal glomerulonephritis
Fever, edema, fatigue, hypertension, Algeria, hematuria
Urinalysis of acute post streptococcal glomerulonephritts
Cloudy, red or brown
- protein ( = casts), blood ( increased ASO titer and BUN), leukocyte esterase positive (need to look at in microscopic)
Microscopic findings of acute Post streptococcal glomerulonephritis
- Increased RBCs, often dymorphic
- Increased WBCs
- increased renal tubular epithelial cells
- Increased casts: RBC, hemoglobin, granular
Normal glomerulus
Post strep glomerulus
Rapidly progressive crescentric (acute nephritic)
- Cellular proliferation in Bowman’s space form crescents: leukocyte infiltration; fibrin deposits; damages to glomerular basement membrane
- Complication of systemic lupus erythematosis
Minimal change disease (acute nephrotic)
Loss of podocyte foot processes; dysfunction of t-cell immunity; follows infections and responsible for most cases of nephrotic syndrome in children; rapid response to steroids
Focal glomerulosclerosis (variable)
Sclerotic damage to limited number of glomeruli with hyaline and lipid deposits and loss of foot processes; focal IgM and C3 deposits. Proteinuria predominant
Changes in glomerular membrane and cellular structures
- Results in varying degrees of hematuria and proteinuria
- thickening of membrane due to deposits of IgG immune complexes
- alteration of cellularity of the capillary walls
- IgA deposits on glomerular membrane 1-2 days following a mucosal infection of respiratory, gastro, or urinary tract infection from infectious agents that stimulate IgA
- disruption and damage of podocytes
Cause of chronic glomerulonephritis
- slow and progressive damage to the glomeruli
- leads tow chronic/end stage renal disease
- impaired GFR
Clinical findings of chronic glomerulonephritis
Edema, azotemia, hypertension, oliguria, hematuria, anemia
Urinalysis of chronic glomerulonephritis
Protein > 2.5g/day, blood, leukocyte esterase positive
Microscopic findings of chronic glomerulonephritis
- Increased RBCs, often dysmorphic
- increased WBCs
- increased renal tubular epithelial cells
- increased casts: all types, particularly granular, waxy, broad
Systemic diseases associated with glomerulonephritis
- Diabetes mellitus
- autoimmune disorders: systemic lupus erythematosus (SLE), sjogren syndrome, Berger disease, IgA
- amyloidosis
- Infections: viral: HIV, HBV bacterial: group A strep, syphilis
- malignancies:multiple myeloma
Cause of acute tubular necrosis (ATN)
Damage to renal tubular epithelium caused by:
- Ischemia due to decreased blood flow and lack of oxygen to RTE cells seen in shock, sepsis, trauma
- toxic substances in urine: exogenous (antibiotics, heavy metals, organic solvents, heron, cocaine, poisons) and endogenous (myoglobin and hemoglobin)
- can cause oliguria and acute renal failure
Urinalysis of acute tubular necrosis (ATN)
Cloudy, red or brown
- protein small, blood positive
Microscopic findings of acute tubular necrosis (ATN)
- Increased RBCs, often dysmorphic
- increased renal tubular epithelial (RTE) cells
- Increased casts: RTE most abundant, hyaline, granular, waxy
Tubular dysfunction examples: Fanconi syndrome
Loss of proximal tubular function
Tubular dysfunction examples: impaired ability to reabsorb specific substances
- Cystinosis and cystinuria amino acids
- glucose, calcium, bicarbonate, sodium, phosphate
Tubular dysfunction examples: renal tubular acidosis
Inability to secrete hydrogen ions so blood is acidic but unable to produce an acid urine
Interstitial disorders: UTI
- Most common renal disease
- lower urinary tract urethra and bladder: contaminated by fecal, to tight clothes. Most common, + leukocyte esterase and ketones
- Upper urinary tract renal pelvis, tubules, interstitium: from antibiotics
Interstitial disorders: cystitis
Ascending bacterial infection of bladder
Interstitial disorders: urethritis
Infection of urethra
Clinical findings of UTI, cystitis, urethntis
Cloudy, odorous
- pH alkaline, protein, blood, leukocyte esterase, nitrite
Microscopic findings for UTI, cystitis, urethritis
- Increased RBCs and WBCs
- increased transitional epithelium cells
- bacteria/yeasts
Urine culture for specific ID
Cause of pyelonephritis
Infection of upper urinary tract tubules/interstitium
- acute and chronic presentation
Clinical findings of pyelonephritis
- Acute sudden onset of lower back pain, urinary frequency, burning, fever, headache, general malaise
- recurrent infections leads to chronic and can progress to renal failure
- obstructions and bladder/ureters reflux
Urinalysis of pyelonephritis
Cloudy, odorous
- protein, blood, leukocyte esterase, nitrite
Microscopic findings of pyelonephritis
- Increased WBCs and WBC casts (also granular, waxy, RTE)
- increased RBCs
- Bacteria
Urine and blood cultures
Cause of acute interstitial nephritis
Allergic inflammation of renal interstitium followed by inflammation of renal tubules in response to certain medications. Must common cause is acute allograft rejection of a transplanted kidney
Clinical findings of acute interstitial nephritis
Sudden onset of renal symptoms, rash, fever develops app. 2 weeks after medication taken
Urinalysis of acute interstitial nephritis
Protein, blood, leukocyte esterase
Microscopic findings of acute interstitial nephritis
- Increased WBCs with eosinophils
- WBC eosinophilic cast may be present
- increased RBCS
- increased RTE cells
What is normal flora and where is it found?
- Candida species
- GI tract and vagina
- normal bacteria flora keep in control
What causes yeasts to proliferate
Antibiotics, pH change, increased glucose in urine
Cause of kidney failure
Failure of kidneys to maintain adequate excretory, regulatory and endocrine function. Mechanism: prerenal, renal, postrenal
Kidney failure results in
- Decrease in GFR and oliguria
- increased nitrogenous concentrations (azotemia)
- disturbance of fluid, acid-base and electrolyte
- miss of up to 85% nephron function
Chronic renal failure leads to
End stage kidney disease, require dialysis or kidney transplant
What is renal lithasis
Kidney stones:
- calculi, solid aggregates of mineral salts, form within the kidney
- calcium base most frequent at 75%
- triple phosphates, uric acid and cystine at 23%
Factors for formation of renal lithiasis (kidney stones)
- Increase in concentrations of chemical salts
- changes in urinary pH
- urinary stasis
- nucleation or initial crystal formation
Clinical findings of renal lithiasis (kidney stones)
Severe pain radiating from lower back to legs; hematuria present in most cases
- small stones can be passed
- larger stones require lithotripsy or surgery
Types of kidney stones
Cystine, calcium, uric acid, struvite
Cystine stone
Calcium stones
Uric acid stones
Struvite stones
